In this model system, BCR-ABL with a mutation (Y177F) at the tyrosine-177 residue – a high affinity-binding site for the Grb2 SH2 domain when phosphorylated [13,14] – induced a T cell leukemia and lymphoma after a prolonged latent period [15-17]. This evidence concerns the gene GRB2 and T-cell leukemia.